# Signaling Molecules and Diagnosis of Cognitive Disorders: Current State and Prospects

**Authors:** Igor Kvetnoy, Oleg Kheyfets, Lazar Safaniev, Vladimir Kheifets, Ekaterina Mironova, Tatiana Kvetnaia, Gianluigi Mazzoccoli, Kiryl Prashchayeu, Anna Gavrilova

PMC · DOI: 10.3390/ijms27010372 · International Journal of Molecular Sciences · 2025-12-29

## TL;DR

This paper reviews signaling molecules that could help diagnose cognitive disorders like Alzheimer's and vascular dementia, highlighting their potential as biomarkers.

## Contribution

The study compiles and evaluates a panel of signaling molecules for their potential as biomarkers in diagnosing cognitive disorders.

## Key findings

- Cumulative changes in signaling molecules reflect neurodegenerative and vascular processes in cognitive disorders.
- Molecular biomarkers like β-amyloid, tau protein, and α-synuclein show promise for clinical use in Alzheimer's and vascular dementia.
- Further validation is needed before these biomarkers can be applied clinically.

## Abstract

Cognitive disorders present significant medical and social challenges nowadays, due to their high prevalence, progressive course and a lack of effective methods for treatment of neurodegenerative diseases and comorbid pathologies. An important area of research is the identification of molecular biomarkers that reflect early pathophysiological changes and facilitate a more accurate biological characterization of cognitive impairment. This study provides an overview of the most relevant signaling molecules for diagnosing cognitive disorders. It presents data on the effectiveness of using comprehensive panels of molecular biomarkers in clinical practice, including β-amyloid, CD34, claudin, DRP1, endothelin-1, NF-kB, PINK1, RAGE, S100, α-synuclein, and tau protein, in patients with Alzheimer’s disease (AD) and vascular dementia (VD). The study results demonstrate that cumulative changes in the expression of signaling molecules reflect various neurodegenerative and vascular-associated biological processes. The data obtained are comparative in nature and require further validation before potential clinical application.

## Linked entities

- **Proteins:** CD34 (CD34 molecule), cldn10e (claudin 10e), CRMP1 (collapsin response mediator protein 1), NFKB1 (nuclear factor kappa B subunit 1), PINK1 (PTEN induced kinase 1), AGER (advanced glycosylation end-product specific receptor), S100A1 (S100 calcium binding protein A1)
- **Diseases:** Alzheimer’s disease (MONDO:0004975), vascular dementia (MONDO:0004648)

## Full-text entities

- **Genes:** CD34 (CD34 molecule) [NCBI Gene 947], PINK1 (PTEN induced kinase 1) [NCBI Gene 65018] {aka BRPK, PARK6}, S100A1 (S100 calcium binding protein A1) [NCBI Gene 6271] {aka S100, S100-alpha, S100A}, UTRN (utrophin) [NCBI Gene 7402] {aka DMDL, DRP, DRP1}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, SNCA (synuclein alpha) [NCBI Gene 6622] {aka NACP, PARK1, PARK4, PD1}, AGER (advanced glycosylation end-product specific receptor) [NCBI Gene 177] {aka RAGE, SCARJ1, sRAGE}, EDN1 (endothelin 1) [NCBI Gene 1906] {aka ARCND3, ET1, HDLCQ7, PPET1, QME}
- **Diseases:** neurodegenerative diseases (MESH:D019636), AD (MESH:D000544), Cognitive Disorders (MESH:D003072), VD (MESH:D015140)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12786006/full.md

## References

52 references — full list in the complete paper: https://tomesphere.com/paper/PMC12786006/full.md

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Source: https://tomesphere.com/paper/PMC12786006